Abnormal heart rhythms are successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, that deliver rhythmic electrical pulses or other anti-arrhythmia therapies to the heart. Early pacemakers delivered stimulation pulses to the heart at a fixed rate. Fixed rate pacing, however, is not physiological in that periods of increased activity or metabolic demand are not accompanied by the normal physiological rise in heart rate. Rate-responsive pacemakers were, therefore, introduced. Rate-responsive pacemakers employ sensors that indicate changes in physical activity or metabolic demand. One commonly used sensor is a piezoelectric element that responds to changes in physical activity. Other sensors used in rate-responsive pacemakers measure blood oxygen levels, pH of the blood, minute volume, respiration rate, or tidal volume. As an increase in the patient's systemic metabolic demand is detected by one or more sensors, device operating parameters controlling the manner in which stimulation is delivered to the heart are adjusted such that the cardiac output better meets the patient's metabolic need. Typically, the stimulation rate and often the interval between atrial contraction and ventricular stimulation are adjusted.
Cardiac pacing of two, three or even all four heart chambers has been found to be potentially beneficial to patients suffering from congestive heart failure. Multi-site stimulation is aimed at resynchronizing the contractions of the heart chambers in an attempt to improve the working efficiency of the heart and the decreased cardiac output associated with congestive heart failure. Thus, cardiac stimulation devices have been proposed that are capable of sensing a parameter correlated to cardiac output. The device then adjusts stimulation parameters in a way that maximizes cardiac output to improve the well-being of a patient in heart failure.
Both rate responsive cardiac stimulation devices and stimulation devices directed at treating congestive heart failure, or the combination of both, improve patient benefit by optimizing stimulation parameters according to the systemic need for increased cardiac output. However, in adjusting stimulation parameters, particularly increasing stimulation rate, the metabolic demand placed on the myocardium itself is increased. Demand-induced myocardial ischemia may result, particularly in patients with coronary artery disease or ischemic cardiomyopathy.
An increased heart rate results mainly in a shortening of the diastolic phase, which is the period during which oxygen is supplied to the heart. An increased stimulation rate will consequently worsen the situation for an ischemic patient. Symptomatic ischemia, that is ischemia resulting in angina pectoris, will force the patient to rest because of the associated pain. The heart rate will decrease allowing the heart to recover from the ischemic episode given a myocardial infarct has not already occurred. However a large portion of cardiac ischemia may be silent, i.e., a state of ischemia that the patient is not aware of because of an absence of symptoms. Prolonged ischemia will result in irreversible injury to the myocardial tissue.
Myocardial ischemia can be detected by observing changes in the ST-segment of an electrocardiogram. Elevation of the ST-segment in relation to the PQ- and TP-segments is a known indication of myocardial ischemia. Thus, ST-segment elevation may be used as a diagnostic marker of myocardial ischemia during cardiac stimulation.
ST-segment changes may be observed using both surface electrocardiogram (ECG) leads or implanted cardiac electrogram (EGM) leads that are located on or in the heart. The sensitivity of ST-segment changes as a marker of myocardial ischemia is dependent on the number and location of the electrodes. ST-segment elevation observed on an EGM using endocardial leads during cardiac catheterization has been found to indicate myocardial ischemia earlier than changes observed on a surface ECG.
Thus, it would be advantageous to use the heart electrodes implanted in, or in proximity to the heart in connection with a cardiac stimulation device for monitoring for changes in the EGM signal that are indicative of myocardial ischemia. Early, reliable detection of myocardial ischemia that prevents sustained, potentially life-threatening, ischemic episodes would enhance the benefit provided to a patient by cardiac stimulation devices. Therefore, it would be desirable to provide a device and method for detecting ST-segment changes with high sensitivity. Furthermore, it is desirable to provide a device capable of responding to detected myocardial ischemia in a way that alleviates the ischemia.